膀胱缺损修复和功能重建是临床上亟待解决的难题，组织工程技术已被用于膀胱修复重建研究，但其成败主要取决于快速血管化情况。前期研究结合文献提示：低氧条件下脂肪干细胞外泌体miR126通过激活内皮细胞的PI3KR2靶基因调控下游PI3K-AKT-mTOR通路，以增强血管化作用。拟研究内容：（1）明确低氧处理的大鼠脂肪干细胞外泌体促进体内和体外血管生成的作用。（2）阐明低氧调控外泌体miRNA126表达的分子机制以及明确外泌体miR126促进体内和体外血管化的作用。（3）阐明外泌体miR126通过靶向PI3KR2调控PI3K-AKT-mTOR通路促进血管化的分子机制。本课题为解决组织工程膀胱快速血管化提出一种新的策略，为最终实现膀胱缺损修复和功能重建奠定了理论基础。

Bladder defect and dysfunction are urgent problems in clinical practice. Tissue engineering technology has been applied for bladder repair research. However, its success mainly depends on the early and rapid angiogenesis. Previous studies combined with literatures suggested that micro-RNA126 in the exosomes of adipose derived stem cells pretreated by hypoxia regulated the PI3K-AKT-mTOR downstream pathway by activating the target gene PI3KR2 of rat endothelial cells, thus enhancing its angiogenesis function. To study: (1) to study the effect of exosomes of rat adipose derived stem cells pretreated by hypoxia on promoting angiogenesis in vivo and in vitro: (2) To elucidate the molecular mechanism of hypoxia regulating the expression of mRNA126 in exosomes and to clarify the role of mRNA126 in promoting angiogenesis in vivo and in vitro. (3) To elucidate the molecular mechanism of exocrine mRNA126 regulating the PI3K-AKT-mTOR pathway by targeting PI3KR2. This project provides a new strategy for the realization of early rapid angiogenesis of tissue-engineered bladder, and lays a theoretical foundation for the final realization of bladder defect repair and functional reconstruction.